Abstract
Size at birth is a critical determinant of life expectancy, and is dependent primarily on the placental supply of nutrients. However, the placenta is not just a passive organ for the materno-fetal transfer of nutrients and oxygen. Studies show that the placenta can adapt morphologically and functionally to optimize substrate supply, and thus fetal growth, under adverse intrauterine conditions. These adaptations help meet the fetal drive for growth, and their effectiveness will determine the amount and relative proportions of specific metabolic substrates supplied to the fetus at different stages of development. This flow of nutrients will ultimately program physiological systems at the gene, cell, tissue, organ, and system levels, and inadequacies can cause permanent structural and functional changes that lead to overt disease, particularly with increasing age. This review examines the environmental regulation of the placental phenotype with particular emphasis on the impact of maternal nutritional challenges and oxygen scarcity in mice, rats and guinea pigs. It also focuses on the effects of such conditions on fetal growth and the developmental programming of disease postnatally. A challenge for future research is to link placental structure and function with clinical phenotypes in the offspring.
Highlights
This review examines the environmental regulation of the placental phenotype with particular emphasis on the impact of maternal nutritional challenges and oxygen scarcity in mice, rats and guinea pigs
In mice and rats fed high-fat diets during pregnancy, the abundances of lipoprotein lipase, fatty acid binding protein, very low-density lipoprotein receptor and/or fatty acid transporter protein are increased in the placenta near term, depending on the content of fat in the diet and whether simple sugars were consumed in excess (Rebholz et al, 2011; Qiao et al, 2012, 2015; Mazzucco et al, 2013; Sferruzzi-Perri et al, 2013; Reynolds et al, 2015)
Identifying the postnatal functional consequences arising from an adverse prenatal environment with a known placental phenotype could aid in the development of placental biomarkers for early diagnosis, assist in identifying susceptible individuals at risk for adult disease, and contribute to the discovery of novel therapeutic strategies to prevent or ameliorate programmed effects
Summary
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